The innate immune system (IIS) is the first line of defense against infectious agents and the detection of tissue damage. The IIS recognizes a group of molecules essential for the survival of microorganisms, which are called pathogen-associated molecular patterns (PAMPs). In addition, IIS recognizes molecules produced and released by damaged or stressed cells, called damage associated molecular patterns (DAMPs). Both PAMPs and DAMPs are recognized by a group of evolutionarily conserved receptors on IIS cells called pattern recognition receptors (PRRs). The recognition of PAMPs and DAMPs by PRRs present in IIS cells leads to different effects on the immune response, including phagocytosis, production of reactive oxygen species (ROS), and expression of genes related to the production of inflammatory and antiviral mediators. For this reason, PRRs are central elements in IIS to respond to pathogens and tissue damage.
The immune response against SARS-CoV-2 is similar to that against other viruses, where the innate immune system acts at early stages through the secretion of type 1 interferon (type 1 IFN), which prevents viral replication and the activation of natural killer (NK) cells. Later, the adaptive immune system acts through CD8+ cytotoxic T-lymphocytes and antibody production, which aim to destroy infected cells and block viral entry into cells. All the above leads to the elimination of the virus and mild symptomatology. However, in individuals with a weakened immune system, the viral infection spreads and leads to a potent inflammatory response, which leads to the recruitment of immune cells to the lungs, where they can cause severe pulmonary and even systemic pathology.
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